C57BL/6JCya-Ndufc2em1flox/Cya
Common Name:
Ndufc2-flox
Product ID:
S-CKO-14096
Background:
C57BL/6JCya
Product Type
Age
Genotype
Sex
Quantity
Price:
Contact for Pricing
Basic Information
Strain Name
Ndufc2-flox
Strain ID
CKOCMP-68197-Ndufc2-B6J-VA
Gene Name
Product ID
S-CKO-14096
Gene Alias
1810004I06Rik; 2010300P09Rik; G1
Background
C57BL/6JCya
NCBI ID
Modification
Conditional knockout
Chromosome
7
Phenotype
Document
Application
--
Note: When using this mouse strain in a publication, please cite “C57BL/6JCya-Ndufc2em1flox/Cya mice (Catalog S-CKO-14096) were purchased from Cyagen.”
Strain Description
Ensembl Number
ENSMUST00000032882
NCBI RefSeq
NM_024220
Target Region
Exon 2~3
Size of Effective Region
~1.9 kb
Detailed Document
Overview of Gene Research
NDUFC2, encoding NADH: ubiquinone oxidoreductase subunit C2, is a subunit of mitochondrial complex I. Mitochondrial complex I is crucial in the oxidative phosphorylation pathway for ATP production, and thus NDUFC2 is important for maintaining normal mitochondrial function and cellular energy metabolism [2,3,4].
In an ischemia-reperfusion injury model, NDUFC2 deficiency decreased antioxidant levels, leading to NLRP3 activation and endothelial mesenchymal transformation (EndoMT) [1]. In a mouse model of complex human disease, Ndufc2 disruption altered complex I assembly and activity, increased reactive oxygen species production and inflammation, and increased stroke susceptibility [3]. In ACS patients, a significant reduction of NDUFC2 expression was detected in circulating mononuclear cells, and in vitro NDUFC2 silencing affected vascular cell viability and angiogenesis while stimulating markers of plaque rupture [4].
In conclusion, NDUFC2 is essential for normal mitochondrial function and energy metabolism. Through gene-knockout or silencing in various models, it has been shown that NDUFC2 deficiency is associated with increased risks of ischemic stroke and acute coronary syndromes, highlighting its potential as a drug target for these diseases [1,3,4].
References：
1. Chen, Jianwei, Liu, Xiaoyu, Bi, Ran, Liu, Pengtao, Gong, Weidong. 2023. NDUFC2 deficiency exacerbates endothelial mesenchymal transformation during ischemia-reperfusion via NLRP3. In Neuroreport, 34, 670-676. doi:10.1097/WNR.0000000000001940. https://pubmed.ncbi.nlm.nih.gov/37506315/
2. Alahmad, Ahmad, Nasca, Alessia, Heidler, Juliana, Ghezzi, Daniele, Taylor, Robert W. 2020. Bi-allelic pathogenic variants in NDUFC2 cause early-onset Leigh syndrome and stalled biogenesis of complex I. In EMBO molecular medicine, 12, e12619. doi:10.15252/emmm.202012619. https://pubmed.ncbi.nlm.nih.gov/32969598/
3. Rubattu, Speranza, Di Castro, Sara, Schulz, Herbert, Hubner, Norbert, Volpe, Massimo. 2016. Ndufc2 Gene Inhibition Is Associated With Mitochondrial Dysfunction and Increased Stroke Susceptibility in an Animal Model of Complex Human Disease. In Journal of the American Heart Association, 5, . doi:10.1161/JAHA.115.002701. https://pubmed.ncbi.nlm.nih.gov/26888427/
4. Raffa, Salvatore, Chin, Xiao Lan Diana, Stanzione, Rosita, Volpe, Massimo, Rubattu, Speranza. 2019. The reduction of NDUFC2 expression is associated with mitochondrial impairment in circulating mononuclear cells of patients with acute coronary syndrome. In International journal of cardiology, 286, 127-133. doi:10.1016/j.ijcard.2019.02.027. https://pubmed.ncbi.nlm.nih.gov/30808603/
Quality Control Standard
Sperm Test
Pre-cryopreservation: Measurement of sperm concentration, determination of sperm viability.
Post-cryopreservation: A vial of cryopreserved sperms is selected for in-vitro fertilization from each batch.
Environmental Standards:SPF
Available Region:Global
Source:Cyagen